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Anti-Tuberculosis Drug Induced Hepatotoxicity and Genetic Polymorphisms in Drug-metabolizing Genes

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Anti-tuberculosis drug induced (ATD) hepatotoxicity is uncommon and unpredictable. It might be related to drug itself or reactive metabolites derived from the drugs in vivo. Several demographic characteristics, such as race, age, sex, body mass index, alcohol intake, have been reported to be susceptibility risk factors for hepatotoxicity related to ATDs. There is now evidence that genetic variations or polymorphisms in biotransformation or detoxification systems controlled by NAT2, GSTM1 etc., might modulate the toxic effects of some drugs. Since prevalences of polymorphisms are different in different ethnic populations, the incidences of ATD hepatotoxicity vary in populations. Thus, knowledge of prevalences of polymorphisms in these genes in a population, prior to medication, may be useful in evaluating the risk and controlling ATD hepatotoxicity.





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Keywords: anti-tuberculosis drugs; cyp genes; gstm1; hepatotoxicity; nat2; polymorphism

Document Type: Review Article

Publication date: June 1, 2003

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  • Current Pharmacogenomics provides comprehensive overviews of all current research on pharmacogenomics and pharmacogenetics. All areas of the field from pre-clinical to clinical research are covered, including related areas such as genomics, proteomics, target discovery, bioinformatics and novel diagnostics. This international journal is peer-reviewed and publishes both mini- and full review articles.

    The journal has become essential reading for all researchers and clinicians with interests in pharmacogenomics and pharmacogenetics.
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